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Frozen shoulder (adhesive capsulitis)

Frozen shoulder: an inflammatory fibrosis of the capsule with progressive painful stiffness. The phases, realistic timelines and what helps at each.

The essentials, in 30 seconds

A loss of passive external rotation greater than 50 % suggests frozen shoulder, with treatment adapted to the phase of the condition.

What it is
An inflammatory fibrosis of the glenohumeral capsule, with a progressive, painful loss of both active and passive mobility.
Who gets it
2 to 5 % of the population is affected, mostly women aged 40 to 60, with diabetes the main risk factor.
How to decide
Clinical diagnosis: passive external rotation must be reduced by more than 50 % compared with the healthy side.
What to do first
Treatment matched to the phase, combining education, gentle exercise, manual therapy and corticosteroid injections.
How long
Three phases over 1 to 3 years; about 40 % of patients still have symptoms in the long term, most often mild.

What follows covers each of these points in detail, with sources. It is there if you need it.

This topic is taught in a course: L’épaule : immersion clinique et communication, online with Germain Delos.

Chapter by chapter

1 / 8

7 article chapters · 40 min in total

Chapter 1

Understanding◔ 6 min

Frozen shoulder is an inflammatory fibrosis promoted by diabetes, affecting 2 to 5 % of the population.

Prevalence
Between 2 and 5 % of the population is affected, mostly women aged 40 to 60.
Phases
The course runs through three phases over 1 to 3 years; about 40 % of patients still have symptoms, most often mild.
Mechanism
The capsule thickens under the effect of synovitis, then capsular fibrosis.
History
Described since 1934 by Codman, frozen shoulder remains poorly understood in pathophysiological terms.
Chapter 2

Diagnosing◔ 7 min

Diagnosis is clinical: the cardinal sign is a loss of passive external rotation greater than 50 %.

History-taking
Onset is insidious, with no trauma, worsening gradually over several weeks.
Cardinal sign
Loss of passive external rotation greater than 50 % is the cardinal sign.
Criteria
The Walmsley consensus describes the early stage through pain and a global loss of active and passive range.
Chapter 3

Treating◔ 9 min

Treatment is staged: education and injection first, surgery only after 6 to 9 months.

Hierarchy
Early intra-articular corticosteroid injection, accompanied by home exercises, gives the best short-term outcomes.
Exercise
Staying gentle and progressive avoids reactivating inflammation through excessive pain.
Injection
In phase 1, the most painful, corticosteroid injections are an option, as a conditional recommendation.
Education
Reassuring about the benign nature of the condition is part of patient education, outside red flags.
Chapter 4

Diabetes◔ 5 min

Diabetes multiplies the risk by about 5, with a more severe, treatment-resistant picture.

Mechanism
Hyperglycaemia forms advanced glycation end-products that stiffen capsular collagen.
Prevalence
Frozen shoulder affects 13.4 % of people with diabetes, against 2 to 5 % in the general population.
Duration
The risk rises with the duration of diabetes, especially beyond 10 years.
Chapter 5

Recovery◔ 4 min

About 40 % of patients still have symptoms, most often mild, and return to sport follows functional criteria, not a fixed timescale.

Self-management
Guided by the physiotherapist, self-management is the pillar of durable recovery.
Contralateral
The opposite shoulder is affected in 6 to 17 % of cases, especially in people with diabetes.
HEP programme
The exercise programme respects the pain threshold, adjusted by the 24-hour rule.
Return to sport
Objective functional criteria, not a fixed timescale, decide the return to sport.
Chapter 6

Clinical cases◔ 4 min

Acute onset with muscle wasting and motor deficit should rule out a diagnosis of frozen shoulder.

Classic case
The Phansopkar 2023 case describes a 57-year-old man whose shoulder improved under physiotherapy.
Diagnostic trap
Disproportionate motor weakness should raise suspicion of Parsonage-Turner rather than frozen shoulder (Ohta 2017).
Chapter 7

In practice◔ 5 min

Refer to a physician in cases of red flags or stalled progress, and measure outcomes with validated PROMs.

Referral
Stalled progress at 3-6 months despite well-conducted physiotherapy justifies the surgeon's opinion.
Collaboration
The diabetologist is involved for a poorly controlled patient, the psychologist for catastrophising.
PROMs
SPADI and QuickDASH are the most practical questionnaires to use in clinic.
Barriers to EBP
Lack of time and difficult access to the literature are overcome by audit and feedback.
8

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Anthony BAILLON

Physiotherapist


Physiotherapy - Shoulder

In brief

Frozen shoulder, or adhesive capsulitis, is an inflammatory fibrosis of the glenohumeral capsule causing a progressive, painful loss of both active and passive shoulder movement. It affects 2 to 5 % of the population, above all women aged 40 to 60, with diabetes the main systemic risk factor. It runs through three phases (freezing, frozen, thawing) over one to three years. Diagnosis is clinical, the cardinal sign being a loss of passive external rotation greater than 50 % of the healthy side. Treatment, matched to the phase, combines education, gentle exercise, manual therapy and intra-articular corticosteroid injections.

Clinical synthesis based on the landmark review Millar 2022 Nature Reviews, the UK FROST trial 2020 Lancet, the network meta-analysis Challoumas 2020 JAMA Network Open and the 2023-2026 data on the diabetic subgroup.

Diagnosis Conservative treatment Diabetes & FS Evidence-based
2-5%
Prevalence in the general population
Millar 2022 NRDP
38%
Prevalence in people with diabetes
Zreik 2016 MLTJ - MA
>50%
Loss of passive external rotation (the cardinal sign)
Kelley 2013 JOSPT CPG

Clinical summary

  • Frozen shoulder is an inflammatory fibrosis of the glenohumeral capsule affecting 2 to 5 % of the population, mainly women between 40 and 60. It may be primary and idiopathic, or secondary (after trauma, surgery or immobilisation).
  • Above all, diabetes mellitus is the main systemic risk factor (prevalence 10-38 %, with more severe and more treatment-resistant forms). Thyroid disorders, above all hypothyroidism, are a second axis (Chuang JSES 2023 meta-analysis).
  • The condition runs through 3 overlapping phases : a painful phase (freezing, 2-9 months), a stiff phase (frozen, 4-12 months), and a thawing phase (5 months to more than 2 years). The natural history is long (1-3 years), but about 40 % of patients still have symptoms in the long term, most often mild.
  • Diagnosis is clinical. The cardinal sign: a symmetrical loss of both active AND passive range, in particular passive external rotation reduced by more than 50 % against the healthy side (Kelley 2013).
  • Plain radiography serves above all for the differential diagnosis (glenohumeral osteoarthritis, calcific tendinopathy, the sequelae of a fracture). MRI can support the diagnosis by showing thickening of the coracohumeral ligament and enhancement of the rotator interval and of the axillary capsule (Suh 2019 meta-analysis).
  • Treatment is progressive and matched to the phase. Patient education and reassurance are fundamental. Corticosteroid injections into the joint are effective on pain in the short term (Challoumas 2020 NMA, Sun 2017 MA).
  • Gentle, progressive exercise is the basis of treatment (Cochrane Page 2014). Manual therapy alongside it improves mobility and function (Noten 2016, Yang 2007).
  • The major randomised trial UK FROST (Rangan 2020 Lancet) shows that early structured physiotherapy, manipulation under anaesthetic and arthroscopic capsular release give comparable functional results at 12 months, with physiotherapy remaining the most cost-effective.
  • For resistant cases (particularly in people with diabetes), arthrographic hydrodilatation under ultrasound guidance (Dimitri-Pinheiro 2022) can create a window of opportunity to restart rehabilitation.
  • Recurrence on the same side is rare (under 5 %), but the other shoulder is affected in 6 to 17 % of patients within 5 years, with an excess risk in people with diabetes.
  • The return to sport should rest on objective functional criteria (range and strength above 90 % of the healthy side, no pain, scapulohumeral control) rather than on a fixed calendar.
  • Medical referral is required where red flags are present (reasoning transposed from Finucane 2020): non-mechanical night pain, disproportionate motor weakness, a history of cancer, a neurological sign.
  • Measuring outcomes with PROMs (SPADI, DASH, ASES, Constant-Murley) is essential for making progress objective and adapting management.

Contents

  1. What are the fundamentals to know about frozen shoulder (adhesive capsulitis)?
    1. How is this condition defined, who does it affect and what are the risk factors?
    2. What happens in the joint capsule, and how does the condition evolve naturally?
  2. How do you assess and diagnose frozen shoulder (adhesive capsulitis) with certainty?
    1. Which questions should you ask to understand the patient and their history?
    2. Which clinical tests should you perform, and which other conditions should you rule out?
    3. Should patients be classified into stages, and what are the benefits?
  3. Which treatment strategies are the most effective for frozen shoulder (adhesive capsulitis)?
    1. Where do you start? What is the recommended hierarchy of interventions?
    2. What is the place of exercise and of manual therapy?
    3. Injections, hydrodilatation, surgery: when should you escalate?
    4. Beyond the physical: how do you educate the patient and address psychological factors?
  4. Frozen shoulder and diabetes: why does this subgroup deserve particular attention?
    1. What are the biological mechanisms linking diabetes and frozen shoulder?
    2. How do you stratify risk and adapt management in the patient with diabetes?
  5. How do you secure lasting recovery and prevent recurrence of frozen shoulder (adhesive capsulitis)?
    1. How do you make the patient an active participant in their recovery through self-management?
    2. When and how should a safe return to sport and to activity be planned?
  6. What do real clinical cases teach us about frozen shoulder (adhesive capsulitis)?
    1. Analysis of a “classic” case: from assessment to resolution.
    2. The diagnostic challenge: when frozen shoulder mimics another condition.
    3. A complex case: resistant frozen shoulder in a patient with diabetes.
  7. How do you apply these recommendations concretely in your practice?
    1. When and to which other health professionals should you refer?
    2. How do you measure outcomes and overcome barriers to implementation?

What are the fundamentals to know about frozen shoulder (adhesive capsulitis)?

In this chapter: the contemporary definition of frozen shoulder, consolidated epidemiology (Millar 2022 NRDP, Cucchi 2017), the dominant risk factors (diabetes, thyroid disorders: Zreik 2016 MA, Chuang 2023 MA), the inflammation-fibrosis pathophysiology mediated by TGF-beta, and the natural trajectory in 3 phases with long-term residual impairment.

Frozen shoulder, known in English as frozen shoulder or adhesive capsulitis, is a painful and disabling condition characterised by a progressive, substantial loss of active and passive movement at the glenohumeral joint. Recognised since 1934 (Codman), it paradoxically remains poorly understood in aetiopathogenic terms, as the landmark review Millar 2022, published in Nature Reviews Disease Primers, points out.1

How is this condition defined, who does it affect and what are the risk factors?

Frozen shoulder is defined as an inflammatory fibrosis of the glenohumeral joint capsule, causing thickening and retraction of the capsule and a painful restriction of movement.1,2 Its prevalence in the general population is estimated at between 2 % and 5 %, affecting women preferentially (OR about 1.6) between 40 and 60 years.1 Idiopathic forms are the most frequent, but secondary forms occur after trauma, shoulder surgery (particularly of the cuff) or prolonged immobilisation.3

2-5 %Prevalence in the general population
10-38 %Prevalence in people with diabetes
x1.6OR women vs men
40-60Peak age of incidence

Prevalence compared: general population vs people with diabetes

Diabetes multiplies the risk of frozen shoulder by about 5 (Zreik 2016: 95 % CI 3.2-7.7)

Frozen shoulder prevalence 2 to 5 per cent in the general population versus 10 to 38 per cent in people with diabetes 40% 30% 20% 10% 0% 2-5 % General population 10-38 % Patients with diabetes x5 the risk

Source: Zreik NH et al. Muscles Ligaments Tendons J 2016;6(1):26-34. PMID 27331029 - a meta-analysis of 12 studies. Chen MH, Chen WS. J Clin Med 2024;13(19):5696. PMID 39407755.

Several systemic and local risk factors are clearly established. The most powerful and best documented is diabetes mellitus (T1DM and T2DM), with a prevalence reaching 10 to 38 % across series, and forms that are consistently more severe and more resistant to treatment.4,5 Thyroid disorders are the second axis: the Chuang 2023 meta-analysis (10 case-control studies, 127,967 patients, JSES) finds more thyroid disease in patients with frozen shoulder (OR 1.87; 95 % CI 1.37-2.57), significantly so for hypothyroidism (OR 1.92) and subclinical hypothyroidism (OR 2.56), but not for hyperthyroidism (OR 1.42; 95 % CI 0.63-3.22).6

Systemic risk factors for frozen shoulder (adjusted OR/RR)

A synthesis of the 2016-2024 meta-analyses - the values are pooled estimates

Frozen shoulder risk factors OR=1 2 3 4 5 Diabetes OR ~5 Dupuytren's disease OR ~3 Thyroid dysfunction OR ~1.9 Women vs men OR ~1.6

Sources: Zreik 2016 MLTJ - Chuang 2023 JSES - Cucchi 2017 Joints - Millar 2022 NRDP.

Other important risk factors include Dupuytren's disease (a robust association suggesting a genetic predisposition to fibrosis), prolonged immobilisation after a fracture or chest or breast surgery, certain drugs (protease inhibitors, fluoroquinolones) and dyslipidaemia.1,7

What happens in the joint capsule, and how does the condition evolve naturally?

Axial and sagittal shoulder MRI: thickened and twisted coracohumeral ligament, arrows on the ligament, adhesive capsulitis.

MRIAxial and sagittal shoulder MRI: thickened and twisted coracohumeral ligament, arrows on the ligament, adhesive capsulitis.

Source : Zhao et al., PloS one, 2012, figure 2 · CC BY

The pathophysiology is a complex process combining synovial inflammation and capsular fibrosis. The early phase is marked by a hypervascular synovitis, with angiogenesis and an inflammatory infiltrate rich in mast cells, M2 macrophages and T lymphocytes.1,8 The pro-inflammatory cytokines (IL-6, TNF-alpha) activate fibroblasts, which transform into myofibroblasts. These produce a disordered extracellular matrix rich in type I and III collagen, under the control of TGF-beta, the main mediator of capsular fibrosis.1,9

This cascade leads to characteristic thickening at the coracohumeral ligament, the axillary recess and the rotator interval, progressively restricting joint volume.1,10 In patients with diabetes, advanced glycation end-products (AGEs) interact with collagen and amplify capsular stiffness, which partly explains the more severe forms seen in this population.11

The natural course in 3 phases (Reeves 1975, updated Millar 2022)

Overlapping phases - a typical total duration of 1 to 3 years

Phases of frozen shoulder Phase 1 - Freezing 2 to 9 months Pain dominates Phase 2 - Frozen 4 to 12 months Maximal stiffness Phase 3 - Thawing 5 months to 2+ years Slow recovery Synovial inflammation Angiogenesis Night pain ++ Maximal fibrosis ER lost >50 % Pain reduced Remodelling ROM gained Function restored A temporal continuum

Source: Reeves B 1975, Hannafin JA, Chiaia TA 2000, updated Millar NL et al. Nat Rev Dis Primers 2022;8:59. PMID 36075904.

The natural history is traditionally described as self-limiting, but that idea needs qualifying. The Hand 2008 study (223 patients, 269 shoulders, mean follow-up 4.4 years) found that 59 % of patients had normal or near-normal shoulders and 41 % reported persistent symptoms; these symptoms were mild in 94 % of cases and severe, with pain and functional loss, in 6 %, the outlook being worse the more severe the initial presentation.13 The retrospective series of Vastamäki 2012 (83 patients, follow-up 2 to 27 years) is more favourable: in untreated patients, range of motion returned to the level of the unaffected side in 94 % of cases, and 51 % were entirely pain-free.12 The Wong 2017 meta-analysis confirms these data and identifies the adverse prognostic factors: diabetes, initial severity, depression and involvement of the dominant arm.14

Treating frozen shoulder as strictly self-limiting is a simplification: at a mean of 4 years, about 4 patients in 10 still have symptoms, most often mild.

Key points

  • Frozen shoulder is an inflammatory fibrosis of the glenohumeral capsule affecting 2 to 5 % of the population (Millar 2022 NRDP).
  • Above all, diabetes is the main systemic risk factor (OR ~5, prevalence 10 to 38 %); thyroid dysfunction and Dupuytren's disease are well-documented secondary factors.
  • The pathophysiology combines hypervascular synovitis and TGF-beta mediated fibrosis.
  • The course runs through 3 phases (freezing, frozen, thawing) over 1 to 3 years, but about 40 % of patients still have symptoms in the long term, most often mild.
Bibliography
  1. Millar NL, Meakins A, Struyf F, et al. Frozen shoulder. Nat Rev Dis Primers. 2022;8(1):59. PMID 36075904.
  2. Cho CH, Bae KC, Kim DH. Treatment Strategy for Frozen Shoulder. Clin Orthop Surg. 2019;11(3):249-257. PMID 31475043.
  3. Lewis J. Frozen shoulder contracture syndrome - Aetiology, diagnosis and management. Man Ther. 2015;20(1):2-9. PMID 25107826.
  4. Huang YP, Fann CY, Chiu YH, et al. Association of diabetes mellitus with the risk of developing adhesive capsulitis. Arthritis Care Res. 2013;65(7):1197-1202. DOI 10.1002/acr.21938.
  5. Zreik NH, Malik RA, Charalambous CP. Adhesive capsulitis of the shoulder and diabetes: a meta-analysis of prevalence. Muscles Ligaments Tendons J. 2016;6(1):26-34. PMID 27331029.
  6. Chuang SH, Chen YP, Huang SW, Kuo YJ. Association between adhesive capsulitis and thyroid disease: a meta-analysis. J Shoulder Elbow Surg. 2023;32(6):1314-1322. PMID 36871608.
  7. Cucchi D, Marmotti A, De Giorgi S, et al. Risk Factors for Shoulder Stiffness: Current Concepts. Joints. 2017;5(4):217-223. PMID 29270559.
  8. Ryan V, Brown H, Minns Lowe CJ, Lewis JS. The pathophysiology associated with primary (idiopathic) frozen shoulder: A systematic review. BMC Musculoskelet Disord. 2016;17:340. PMID 27527912.
  9. Rodeo SA, Hannafin JA, Tom J, Warren RF, Wickiewicz TL. Immunolocalization of cytokines and their receptors in adhesive capsulitis of the shoulder. J Orthop Res. 1997;15(3):427-436. PMID 9246090.
  10. Hagiwara Y, Ando A, Onoda Y, et al. Coexistence of fibrotic and chondrogenic process in the capsule of idiopathic frozen shoulders. Osteoarthritis Cartilage. 2012;20(3):241-249. PMID 22233812.
  11. Chen MH, Chen WS. A Narrative Review of Adhesive Capsulitis with Diabetes. J Clin Med. 2024;13(19):5696. PMID 39407755.
  12. Vastamaki H, Kettunen J, Vastamaki M. The natural history of idiopathic frozen shoulder: a 2- to 27-year followup study. Clin Orthop Relat Res. 2012;470(4):1133-1143. PMID 22090356.
  13. Hand C, Clipsham K, Rees JL, Carr AJ. Long-term outcome of frozen shoulder. J Shoulder Elbow Surg. 2008;17(2):231-236. PMID 17993282.
  14. Wong CK, Levine WN, Deo K, et al. Natural history of frozen shoulder: fact or fiction? A systematic review. Physiotherapy. 2017;103(1):40-47. DOI 10.1016/j.physio.2016.05.009.

How do you assess and diagnose frozen shoulder (adhesive capsulitis) with certainty?

In this chapter: a targeted history, the cardinal sign of lost passive external rotation, the Walmsley 2009 consensus criteria and the Kelley 2013 JOSPT CPG, a rigorous differential diagnosis and a reasoned place for imaging (radiography, MRI after Suh 2019, ultrasound).

Diagnosing frozen shoulder is essentially clinical. It rests on identifying a specific pattern of restricted glenohumeral movement, combined with actively excluding other conditions that can mimic the picture.1,2 The official clinical practice guidelines of the American Physical Therapy Association (Kelley 2013 JOSPT, evidence level A) remain the international reference.3

Which questions should you ask to understand the patient and their history?

The history points strongly towards the diagnosis from the first consultation. The cardinal elements to look for are:

  • Chronology : typically an insidious onset, with no triggering trauma, worsening gradually over several weeks to months.1,3
  • Pain profile : diffuse shoulder pain, often referred to the deltoid, worse at night and on rapid movement. Night pain is very frequent in the early phase but should not cause concern in the absence of other red flags.3
  • Progressive functional limitation : difficulty doing one's hair, fastening a bra, reaching a back pocket or an object overhead.4
  • Comorbidities to look for actively : diabetes mellitus (HbA1c, duration), thyroid dysfunction, Dupuytren's disease, a history of immobilisation, chest or breast surgery.5,6
  • Medication review : statins, protease inhibitors, fluoroquinolones and aromatase inhibitors have all been described.5

Which clinical tests should you perform, and which other conditions should you rule out?

Oblique sagittal shoulder MRI, T1 sequence: complete obliteration of the fat surrounding the coracohumeral ligament (arrows), a sign of frozen shoulder.

MRIOblique sagittal shoulder MRI, T1 sequence: complete obliteration of the fat surrounding the coracohumeral ligament (arrows), a sign of frozen shoulder.

Source : Li et al., PloS one, 2011, figure 4 · CC BY

The physical examination aims to confirm the symmetrical loss of both active AND passive range at the glenohumeral joint, which is the cardinal sign of frozen shoulder.3,7

The Walmsley 2009 Delphi consensus (70 experts, three rounds) describes the early stage of primary frozen shoulder: marked night pain, pain with rapid or unguarded movement, discomfort lying on the affected shoulder, pain easily aggravated by movement, a global loss of active and passive range with end-range pain in all directions, and onset after the age of 35. The authors stress that these signs have limited ability to distinguish frozen shoulder from other shoulder conditions.7 Common operational definitions add:

  • A loss of passive range of at least 25 % in at least 2 planes of movement compared with the healthy side.
  • A loss of passive external rotation greater than 50 % (or less than 30 degrees in absolute terms) with the elbow at the side.
  • A symmetrical limitation of active and passive movement (unlike cuff conditions).

Diagnostic decision algorithm

After the Kelley 2013 JOSPT CPG and the Walmsley 2009 criteria

Frozen shoulder diagnostic flow chart Shoulder pain + stiffness insidious onset Examination: active AND passive range Passive ER with the elbow at the side, ABD, FLEX Passive ER lost by > 50 % vs the healthy side? + passive loss >= 25 % in 2 planes YES NO Frozen shoulder likely Radiograph to exclude osteoarthritis - calcification - old fracture Another diagnosis Cuff / impingement / osteoarthritis Acromioclavicular / cervical If the presentation is atypical: MRI (Suh 2019)

Source: Kelley MJ et al. JOSPT 2013;43(5):A1-A31 (APTA CPG) PMID 23636125. Walmsley S et al. Phys Ther 2009;89:906-917 PMID 19589853.

The differential diagnosis is fundamental. The main conditions to rule out are:

  • Rotator cuff conditions : tendinopathy, partial or massive tears. Passive movement is generally preserved, unlike in frozen shoulder. Jobe test, lift-off, bear hug, a painful arc in abduction (60-120 degrees).1
  • Glenohumeral osteoarthritis : similar stiffness, but the radiograph reveals joint space narrowing and osteophytes. The population is often older (> 60 years).2
  • Calcific tendinopathy : very acute pain, calcification visible on the radiograph. An intense resorptive phase is possible.8
  • Parsonage-Turner syndrome (neuralgic amyotrophy): disproportionate motor weakness, early muscle wasting, an abnormal EMG.9
  • Cervical radicular conditions : neurological signs (paraesthesia, motor deficit in a root distribution), a positive Spurling test.1
  • Rare causes still worth considering : primary or metastatic tumour of the shoulder, septic arthritis, polymyalgia rheumatica (in older patients).10
  • Missed posterior dislocation : after direct trauma, an epileptic seizure, an electric shock or electroconvulsive therapy. More than half of these dislocations go unnoticed at the first examination and are often mistaken for frozen shoulder. Blocked external rotation in this context calls for medical referral for imaging.13

Red flags - immediate medical referral

  • Non-mechanical night pain, not relieved by changing position.
  • Unexplained weight loss, fever, night sweats, marked fatigue.
  • A personal history of cancer (breast, lung, prostate, kidney, melanoma, thyroid).
  • Motor weakness out of proportion to the loss of passive movement (think Parsonage-Turner, neurological involvement).
  • Visible, rapid muscle wasting.
  • Intense local inflammatory signs (heat, erythema, swelling) - rule out septic arthritis.
  • Complete failure after 6 months of well-conducted management - a diagnostic reassessment is imperative.
  • Stiffness that appeared after an epileptic seizure, an electric shock or trauma : rule out a missed posterior dislocation.

Should patients be classified into stages, and what are the benefits?

Clinical staging by Reeves's phases (freezing, frozen, thawing), updated by Hannafin & Chiaia 2000 and then Millar 2022, remains useful for guiding treatment and managing the patient's expectations, even though this is a continuum rather than a set of discrete stages.1,11

PhaseDurationDominant featureTreatment strategy
Phase 1 - Freezing (painful)2-9 monthsIntense pain, above all at night. Progressive stiffness.Education, pain control, gentle mobilisations, intra-articular corticosteroids if severe (Challoumas 2020).
Phase 2 - Frozen (stiff)4-12 monthsMaximal stiffness. Pain at end range. ER < 30 degrees.End-range manual therapy + progressive stretching + a home exercise programme.
Phase 3 - Thawing (recovery)5-24+ monthsProgressive improvement in ROM and function. Pain has almost gone.Functional strengthening, return to activity, prevention of contralateral recurrence.
A loss of passive external rotation greater than 50 % compared with the healthy side remains the most reliable clinical sign. Any preserved passive ER should prompt the diagnosis to be reconsidered.

Key points

  • Diagnosis is essentially clinical, based on a symmetrical loss of active and passive range.
  • The cardinal sign is a loss of passive external rotation with the elbow at the side greater than 50 % of the other side.
  • The Walmsley 2009 consensus criteria and the Kelley 2013 JOSPT (APTA) recommendations are the references.
  • Imaging (plain radiography, MRI after Suh 2019 where the presentation is atypical, ultrasound) serves above all for the differential diagnosis.
  • Actively look for the comorbidities: diabetes, thyroid dysfunction, Dupuytren's.
  • Know the red flags (non-mechanical night pain, a history of cancer, disproportionate motor weakness) so that referral is prompt.
Bibliography
  1. Lewis J. Frozen shoulder contracture syndrome - Aetiology, diagnosis and management. Man Ther. 2015;20(1):2-9. PMID 25107826.
  2. Cho CH, Bae KC, Kim DH. Treatment Strategy for Frozen Shoulder. Clin Orthop Surg. 2019;11(3):249-257. PMID 31475043.
  3. Kelley MJ, Shaffer MA, Kuhn JE, et al. Shoulder pain and mobility deficits: adhesive capsulitis. J Orthop Sports Phys Ther. 2013;43(5):A1-A31. PMID 23636125.
  4. Le HV, Lee SJ, Nazarian A, Rodríguez EK. Adhesive capsulitis of the shoulder: review of pathophysiology and current clinical treatments. Shoulder Elbow. 2017;9(2):75-84. PMID 28405218.
  5. Cucchi D, Marmotti A, De Giorgi S, et al. Risk Factors for Shoulder Stiffness: Current Concepts. Joints. 2017;5(4):217-223. PMID 29270559.
  6. Chuang SH, Chen YP, Huang SW, Kuo YJ. Association between adhesive capsulitis and thyroid disease: a meta-analysis. J Shoulder Elbow Surg. 2023;32(6):1314-1322. PMID 36871608.
  7. Walmsley S, Rivett DA, Osmotherly PG. Adhesive capsulitis: establishing consensus on clinical identifiers for stage 1 using the Delphi technique. Phys Ther. 2009;89(9):906-917. PMID 19589853.
  8. Kim MS, Kim IW, Lee S, Shin SJ. Diagnosis and treatment of calcific tendinitis of the shoulder. Clin Shoulder Elb. 2020;23(4):210-216. PMID 33330261.
  9. Ohta R, Shimabukuro A. Parsonage-Turner syndrome in a patient with bilateral shoulder pain: A case report. J Rural Med. 2017;12(2):135-138. PMID 29255532.
  10. Mezian K, Coffey R, Chang KV. Frozen Shoulder. In: StatPearls [Internet]. StatPearls Publishing; 2023. PMID 29489251.
  11. Suh CH, Yun SJ, Jin W, et al. Systematic review and meta-analysis of magnetic resonance imaging features for diagnosis of adhesive capsulitis of the shoulder. Eur Radiol. 2019;29(2):566-577. PMID 29978436.
  12. Hollmann L, Halaki M, Kamper SJ, et al. Does muscle guarding play a role in range of motion loss in patients with frozen shoulder? Musculoskelet Sci Pract. 2018;37:64-68. PMID 29986193.
  13. Rodia F, Ventura A, Touloupakis G, Theodorakis E, Ceretti M. Missed posterior shoulder dislocation and McLaughlin lesion after an electrocution accident. Chin J Traumatol. 2012;15(6):376-378. PMID 23186932.

Which treatment strategies are the most effective for frozen shoulder (adhesive capsulitis)?

In this chapter: a stepped-care approach, a GRADE pyramid of the interventions, exercise and manual therapy (Cochrane Page 2014, Noten 2016), corticosteroid injections (Challoumas 2020 NMA, Sun 2017 MA), hydrodilatation and the reserved place of surgery (UK FROST Rangan 2020 Lancet).

Frozen shoulder has a natural tendency to improve over 1 to 3 years, but its functional impact justifies active management. The 2020-2024 recommendations converge on a stepped multimodal strategy, matched to the phase of the condition and to tissue irritability.1,2

Where do you start? What is the recommended hierarchy of interventions?

The initial approach rests on the triad of education + pain management + physiotherapy. The Challoumas 2020 network meta-analysis (JAMA Network Open, 65 randomised studies, 4,097 participants) compares the non-surgical treatments.3 It associates intra-articular corticosteroid injection, in frozen shoulder of less than one year's duration, with better short-term outcomes than the other non-surgical treatments, with a benefit that may last up to six months; this treatment should be accompanied by a home exercise programme. It could reach no conclusion on surgery, because the included trials did not compare the same interventions.3

A larger network meta-analysis (Meng 2026, BMJ, 189 RCTs, 12,988 participants) concludes, with moderate certainty, that extracorporeal shockwave therapy probably reduces short-term pain compared with usual care and that manipulation under anaesthetic, with or without injection, probably improves short-term flexion; most other estimates are of low or very low certainty, most trials are at high risk of bias, and comparative safety remains highly uncertain.18

Hierarchy of the interventions (an editorial rating applying GRADE principles to the cited sources, not a published assessment)

A synthesis of Challoumas 2020 NMA + UK FROST Rangan 2020 + Cochrane Page 2014 + Meng 2026 NMA

GRADE pyramid of frozen shoulder treatments GRADE HIGH Injection vs control: short-term function and external rotation (pain: moderate certainty) GRADE MODERATE Manipulation under anaesthetic, arthroscopy; shockwave therapy, short-term pain (Meng 2026) GRADE LOW End-range manual therapy, hydrodilatation with injection, supervised exercise, LLLT alone GRADE VERY LOW Therapeutic ultrasound (insufficient evidence - not recommended as routine) NOT RECOMMENDED Passive immobilisation, forced stretching in the inflammatory phase, abrupt manipulation

Sources: Challoumas D et al. JAMA Netw Open 2020;3(12):e2029581 - Rangan A et al. Lancet 2020;396:977-989 - Page MJ et al. Cochrane 2014 - Kelley 2013 JOSPT CPG. Education and reassurance, the foundation of good practice, are not graded.

The pragmatic randomised trial UK FROST (Rangan 2020 Lancet, 503 patients, 3 arms) is a major turning point in the literature: it compares early structured physiotherapy (with or without intra-articular corticosteroids), manipulation under anaesthetic and arthroscopic capsular release. At 12 months, no clinically significant difference is seen on the Oxford Shoulder Score (OSS). Physiotherapy is nonetheless the most cost-effective, and so remains the first-line intervention in primary and secondary care.4

What is the place of exercise and of manual therapy?

Supervised exercise plus a home exercise programme (HEP) is the cornerstone of conservative treatment. The Cochrane review Page 2014 (manual therapy + exercise, 32 RCTs) shows modest but consistent benefits on pain and function, particularly when exercise and manual therapy are combined.5

The principles of application are:6,7

  • Painful phase (freezing) : gentle pendulum exercises, active-assisted mobilisation within pain-free range. Avoid forced stretching, which can reactivate the inflammation.
  • Stiff phase (frozen) : low-load, long-duration stretching (Russell 2014), end-range joint mobilisation (Maitland grade III-IV), a home exercise programme several times a day.
  • Thawing phase : progressive strengthening of the cuff and the scapular stabilisers, a return to functional activities, prevention of contralateral recurrence.

The systematic review by Noten 2016 (APMR, 12 RCTs, 810 patients) concludes that mobilisation has beneficial effects and that the Maitland technique and combined mobilisations seem the ones to favour, on still preliminary evidence; in the only trial that assessed it, high-intensity mobilisation improved the Constant score less than no treatment.8 In a multiple-treatment trial of 28 patients, Yang 2007 found end-range mobilisation and mobilisation with movement (Mulligan) more effective than mid-range mobilisation for mobility and function.9

ModalityLevel of evidenceExpected effectLandmark reference
Education + reassuranceNot graded (good practice; no trial tests it in isolation)Adherence up, anxiety down, catastrophising preventedChester 2018 BJSM (prognostic cohort); Coronado 2020 Pain Rep
Supervised exercise + HEPGRADE lowPain, function, ROMPage 2014 Cochrane (no comparison against placebo)
End-range manual therapyGRADE lowROM (synergistic with exercise)Noten 2016 APMR; Yang 2007 Phys Ther; Lee 2025 (Korean guideline)
Intra-articular corticosteroidsGRADE high (function, external rotation, short term), moderate (pain, short term)Pain, function at 6-12 weeksSun 2017 AJSM MA; Challoumas 2020 NMA
HydrodilatationGRADE lowROM + function, resistant casesLee 2025 (combined with injection); Dimitri-Pinheiro 2022 (retrospective series)
Manipulation under anaestheticGRADE moderateRapid ROM gain, a risk of fracture or dislocationUK FROST Rangan 2020
Arthroscopic capsular releaseGRADE moderateNo clinical superiority at 12 months; more serious adverse eventsUK FROST Rangan 2020
ESWTGRADE moderate (pain, short term)Short-term pain; function: low certaintyMeng 2026 BMJ; Vahdatpour 2014 IJPM
LLLTGRADE lowShort-term pain (heterogeneous data)Mixed data
Therapeutic ultrasoundGRADE very lowNo demonstrated benefitPage 2014 Cochrane

Injections, hydrodilatation, surgery: when should you escalate?

The intra-articular corticosteroid injections are an option, particularly in phase 1 (painful): the 2025 Korean clinical practice guideline suggests considering them, alone or combined with physiotherapy (conditional recommendation, low level of evidence).17 The Sun 2017 meta-analysis (AJSM, 8 RCTs, 416 patients) shows, compared with no injection or a sham injection, a significant reduction in pain at 4-6 weeks and at 12-16 weeks.10 The clinical superiority of ultrasound guidance has not been demonstrated, its use depending on the operator's expertise, and the dose of triamcinolone (20 or 40 mg) is a matter of clinical judgement.17

Arthrographic hydrodilatation (distension with a large volume of saline plus corticosteroid plus anaesthetic under ultrasound or fluoroscopic guidance) is an option for patients who do not respond to 3-6 months of conservative treatment, particularly patients with diabetes. The retrospective study Dimitri-Pinheiro 2022 (PMC9465918) shows reduced but real efficacy in patients with diabetes compared with those without.11

Any surgery (manipulation under anaesthetic or arthroscopic release) remains reserved for failures of maximal conservative management (beyond 6-9 months). UK FROST shows that none of the three arms (physiotherapy with injection, manipulation under anaesthetic, arthroscopic release) is clinically superior at 12 months, the differences remaining below the thresholds set in advance; arthroscopic release carries more serious adverse events (eight, against two after manipulation), which justifies favouring conservative management for its lower invasiveness.4

Beyond the physical: how do you educate the patient and address psychological factors?

Therapeutic education is the indispensable first step. It aims to:2,12

  • Explain the natural history (3 phases, a typical duration of 1-3 years, the possibility of minor residual impairment).
  • Reassure the patient that the condition is not serious (in the absence of red flags).
  • Counter the kinesiophobia and catastrophising that worsen disability (Chester 2018 BJSM).
  • Promote self-management (the home exercise programme, energy management, adapting ADLs).

The scoping review Coronado 2020 (Pain Rep) highlights the value of psychologically informed physiotherapy for patients with yellow flags: catastrophising, fear of movement, low self-efficacy.13

UK FROST transformed our view of treatment: the 3 options (early structured physiotherapy with a corticosteroid injection, manipulation under anaesthetic, arthroscopic release) do not differ to a clinically relevant degree at 12 months on the Oxford Shoulder Score. Because the physiotherapy arm included an injection, the trial does not assess physiotherapy on its own; it remains the first-line intervention because it is the least invasive.

Key points

  • Treatment follows a stepped approach : education + exercise + manual therapy first, intra-articular corticosteroids in the painful phase 1, escalation to hydrodilatation or surgery where it fails after 6-9 months.
  • The meta-analysis Challoumas 2020 (JAMA Netw Open) associates early intra-articular injection, accompanied by home exercises, with the best short-term outcomes.
  • The trial UK FROST (Rangan 2020 Lancet) shows that early structured PT with a corticosteroid injection, MUA and arthroscopic release do not differ to a clinically relevant degree at 12 months: MUA is the most cost-effective, PT the least invasive. The physiotherapy arm included an injection, so the trial says nothing about physiotherapy without injection.
  • Exercise should be gentle and progressive, matched to the phase, without triggering significant pain that would reactivate the inflammation.
  • Manual therapy (Maitland, combined mobilisations) has beneficial effects on preliminary evidence (Noten 2016); end-range mobilisation does better than mid-range mobilisation in a small trial (Yang 2007).
  • Education and attention to psychological factors are essential (Chester 2018, Coronado 2020).
Bibliography
  1. Lewis J. Frozen shoulder contracture syndrome. Man Ther. 2015;20(1):2-9. PMID 25107826.
  2. Cho CH, Bae KC, Kim DH. Treatment Strategy for Frozen Shoulder. Clin Orthop Surg. 2019;11(3):249-257. PMID 31475043.
  3. Challoumas D, Biddle M, McLean M, Millar NL. Comparison of Treatments for Frozen Shoulder: A Systematic Review and Meta-analysis. JAMA Netw Open. 2020;3(12):e2029581. DOI 10.1001/jamanetworkopen.2020.29581.
  4. Rangan A, Brealey SD, Keding A, et al. Management of adults with primary frozen shoulder in secondary care (UK FROST): a multicentre, pragmatic, three-arm, superiority randomised clinical trial. Lancet. 2020;396(10256):977-989. PMID 33010843.
  5. Page MJ, Green S, Kramer S, et al. Manual therapy and exercise for adhesive capsulitis (frozen shoulder). Cochrane Database Syst Rev. 2014;(8):CD011275. PMID 25157702.
  6. Kelley MJ, Shaffer MA, Kuhn JE, et al. Shoulder pain and mobility deficits: adhesive capsulitis. J Orthop Sports Phys Ther. 2013;43(5):A1-A31. PMID 23636125.
  7. Russell S, Jariwala A, Conlon R, et al. A blinded, randomized, controlled trial assessing conservative management strategies for frozen shoulder. J Shoulder Elbow Surg. 2014;23(4):500-507. PMID 24630545.
  8. Noten S, Meeus M, Stassijns G, et al. Efficacy of Different Types of Mobilization Techniques in Patients With Primary Adhesive Capsulitis of the Shoulder: A Systematic Review. Arch Phys Med Rehabil. 2016;97(5):815-825. PMID 26284892.
  9. Yang JL, Chang CW, Chen SY, Wang SF, Lin JJ. Mobilization techniques in subjects with frozen shoulder syndrome: randomized multiple-treatment trial. Phys Ther. 2007;87(10):1307-1315. PMID 17684085.
  10. Sun Y, Zhang P, Liu S, et al. Intra-articular Steroid Injection for Frozen Shoulder: A Systematic Review and Meta-analysis of Randomized Controlled Trials. Am J Sports Med. 2017;45(9):2171-2179. PMID 28298050.
  11. Dimitri-Pinheiro S, Pinto BS, Pimenta M, Neves JS, Carvalho D. Influence of diabetes on response to ultrasound guided hydrodistension treatment of adhesive capsulitis: a retrospective study. BMC Endocr Disord. 2022;22(1):227. PMC9465918.
  12. Maund E, Craig D, Suekarran S, et al. Management of frozen shoulder: a systematic review and cost-effectiveness analysis. Health Technol Assess. 2012;16(11):1-264. PMID 22405512.
  13. Chester R, Jerosch-Herold C, Lewis J, Shepstone L. Psychological factors are associated with the outcome of physiotherapy for people with shoulder pain. Br J Sports Med. 2018;52(4):269-275. PMID 27445360.
  14. Coronado RA, Brintz CE, McKernan LC, et al. Psychologically informed physical therapy for musculoskeletal pain. Pain Rep. 2020;5(5):e847. PMID 33490842.
  15. Vahdatpour B, Taheri P, Zare Zadeh A, Moradian S. Efficacy of extracorporeal shockwave therapy in frozen shoulder. Int J Prev Med. 2014;5(7):875-881. PMID 25104999.
  16. Ramirez J. Adhesive Capsulitis: Diagnosis and Management. Am Fam Physician. 2019;99(5):297-300. PMID 30811157.
  17. Lee BC, Kim BS, Lee BJ, et al. Clinical practice guidelines for diagnosis and non-surgical treatment of primary frozen shoulder. Ann Rehabil Med. 2025;49(3):113-138. PMID 40602400.
  18. Meng J, Liu P, Gomes NS, et al. Interventions for adhesive capsulitis: systematic review and network meta-analysis of randomised controlled trials. BMJ. 2026;395:e101057. PMID 42982479.

Frozen shoulder and diabetes: why does this subgroup deserve particular attention?

A section dedicated to the most exposed and the most difficult subgroup to treat. Biological mechanisms (AGEs, collagen glycation), clinical stratification by HbA1c and duration of diabetes, adapting the protocols, and hydrodilatation as an option when treatment plateaus. A synthesis based on the Chen 2024 review in J Clin Med + Zreik 2016 MA + Dimitri-Pinheiro 2022.

Frozen shoulder in the patient with diabetes is a distinct clinical entity in its frequency, its severity and its resistance to standard treatment. Recognising that specificity is essential for adapting management and setting realistic expectations.1,2

What are the biological mechanisms linking diabetes and frozen shoulder?

The Zreik 2016 meta-analysis (MLTJ, 12 studies) establishes that the prevalence of frozen shoulder reaches 13.4 % in people with diabetes (against 2-5 % in the general population) and, conversely, that about 30 % of patients with frozen shoulder have diabetes (95 % CI 24-37).3 The narrative review Chen 2024 (J Clin Med, PMID 39407755) synthesises the biological mechanisms identified to date:1

  • Advanced glycation end-products (AGEs) : chronic hyperglycaemia leads to the formation of AGEs that bind to the collagen of the joint capsule. These AGE cross-links stiffen the extracellular matrix and resist normal degradation mechanisms.
  • Overexpression of TGF-beta and amplification of the profibrotic signalling pathway in people with diabetes, comparable to what is seen in Dupuytren's disease (another fibrosis associated with diabetes).
  • Microangiopathy : impaired periarticular microcirculation, with tissue hypoxia favouring fibrosis.
  • Chronic low-grade inflammation linked to diabetes (raised CRP, IL-6), which prolongs the synovitic phase.
  • Partial resistance to corticosteroids : a poorer response to intra-articular corticosteroids than in people without diabetes (Dimitri-Pinheiro 2022).

Clinical features specific to the patient with diabetes

A synthesis of Chen 2024 J Clin Med + Mertens 2021 SR

Frozen shoulder specifics in diabetes General population Prevalence 2-5 % Typical duration 1-3 years Good response to intra-articular corticosteroids Contralateral recurrence 6 % Standard PT efficacy Mild residual impairment ~30 % Patient with diabetes Prevalence 13.4 % (x5) Duration often > 3 years Reduced response to intra-articular corticosteroids Contralateral recurrence 17 % Reduced PT efficacy Moderate to severe residual impairment

Sources: Chen MH, Chen WS. J Clin Med 2024;13(19):5696 PMID 39407755 - Zreik NH et al. MLTJ 2016 PMID 27331029 - Dimitri-Pinheiro 2022 PMC9465918.

How do you stratify risk and adapt management in the patient with diabetes?

Clinical stratification helps personalise the prognosis and the treatment plan. Several predictors of severity and resistance are documented:1,4,5

  • Duration of diabetes : the risk rises beyond 10 years.
  • HbA1c > 7.5 % : poor glycaemic control is associated with slower recovery and a higher failure rate.
  • Type 1 diabetes : its own role, like that of prolonged insulin therapy, remains debated (Chen 2024).
  • The presence of other microvascular complications : retinopathy, nephropathy, neuropathy.
  • A bilateral or recurrent form.
Risk profileCharacteristicsAdapted treatment strategy
Low riskT2DM < 5 years, HbA1c < 7 %, no complicationsThe standard protocol (PT + HEP + intra-articular corticosteroids in phase 1). A prognosis close to the general population's.
Intermediate risk5-10 years of diabetes, HbA1c 7-8 %, no major complicationsStrengthen education, intensify the HEP, follow up closely, use intra-articular corticosteroids earlier, consider hydrodilatation at 4-6 months if progress plateaus.
High riskT1DM or T2DM > 10 years, HbA1c > 8 %, microvascular complications, bilateralA multidisciplinary approach (diabetologist + physiotherapist + rheumatologist), early hydrodilatation, escalation to MUA or arthroscopy if progress stalls at 6-9 months.

Red flags specific to the patient with diabetes

  • Marked local inflammatory signs plus fever: think septic arthritis (people with diabetes are at increased risk).
  • Associated calcific tendinopathy : more frequent in people with diabetes, and it can complicate the picture.
  • Simultaneous bilateral frozen shoulder : rule out an underlying systemic condition (in particular associated thyroid dysfunction, late-onset JIA).
  • Paradoxical worsening after intra-articular corticosteroids : an infection risk, but also the possibility of avascular necrosis (rare).
  • Persistently poor glycaemic control : to be addressed actively with the general practitioner or diabetologist (hyperglycaemia can be transiently worsened by intra-articular corticosteroids).

Ultrasound-guided hydrodilatation is an option of choice in the patient with diabetes and resistant frozen shoulder. The Mezian StatPearls review and the Dimitri-Pinheiro 2022 study (PMC9465918) show that it allows rehabilitation to be restarted in about 50-70 % of patients who stall despite 3-6 months of well-conducted PT, with a favourable safety profile.4 Important: tell the patient with diabetes about the transient risk of hyperglycaemia after a corticosteroid injection (peak effect at 24-72 h) and coordinate with their general practitioner about adjusting insulin if needed.1

In the patient with diabetes, frozen shoulder is not only more frequent: it is more severe, longer and more resistant. Stratifying risk by HbA1c and duration of diabetes makes it possible to step up the intensity of intervention early.

Key points

  • Diabetes multiplies the risk of frozen shoulder by about 5 (Zreik 2016 MA: 95 % CI 3.2-7.7).
  • The specific biological mechanisms include advanced glycation end-products (AGEs), overexpression of TGF-beta and microangiopathy.
  • The clinical picture in diabetes is more severe, prolonged and resistant to standard treatment.
  • Stratifying by HbA1c and duration of diabetes guides the escalation of treatment.
  • Ultrasound-guided hydrodilatation is an option of choice where progress plateaus at 3-6 months of PT.
  • Coordinate with the diabetologist about glycaemic adjustment around the injection.
Bibliography
  1. Chen MH, Chen WS. A Narrative Review of Adhesive Capsulitis with Diabetes. J Clin Med. 2024;13(19):5696. PMID 39407755.
  2. Millar NL, Meakins A, Struyf F, et al. Frozen shoulder. Nat Rev Dis Primers. 2022;8(1):59. PMID 36075904.
  3. Zreik NH, Malik RA, Charalambous CP. Adhesive capsulitis of the shoulder and diabetes: a meta-analysis of prevalence. Muscles Ligaments Tendons J. 2016;6(1):26-34. PMID 27331029.
  4. Dimitri-Pinheiro S, Pinto BS, Pimenta M, Neves JS, Carvalho D. Influence of diabetes on response to ultrasound guided hydrodistension treatment of adhesive capsulitis: a retrospective study. BMC Endocr Disord. 2022;22(1):227. PMC9465918.
  5. Huang YP, Fann CY, Chiu YH, et al. Association of diabetes mellitus with adhesive capsulitis. Arthritis Care Res. 2013;65(7):1197-1202. DOI 10.1002/acr.21938.
  6. Mezian K, Coffey R, Chang KV. Frozen Shoulder. StatPearls. 2023. PMID 29489251.
  7. Le HV, Lee SJ, Nazarian A, Rodríguez EK. Adhesive capsulitis of the shoulder. Shoulder Elbow. 2017;9(2):75-84. PMID 28405218.

How do you secure lasting recovery and prevent recurrence of frozen shoulder (adhesive capsulitis)?

In this chapter: self-management guided by the physiotherapist, the central role of education about the natural history, prevention of contralateral involvement (a 6-17 % risk), and functional criteria for the return to sport (rather than arbitrary timescales).

Frozen shoulder is often presented as a self-limiting condition, which can lead to underestimating the importance of structured management. Yet, as Hand 2008 showed, about 40 % of patients still have symptoms in the long term, most often mild.2 A well-conducted secondary prevention programme is therefore essential.

How do you make the patient an active participant in their recovery through self-management?

Self-management (self-management) guided by the physiotherapist is the pillar of durable recovery. It rests on three pillars:3,4

  1. Education about the natural history : explain the 3 phases, the typical duration (1-3 years), how rare recurrence on the same side is (under 5 %) but the risk of contralateral involvement (6-17 % according to Wong 2017, above all in people with diabetes).
  2. A home exercise programme (HEP) :
    • Done several times a day (3-5 sessions of 10-15 minutes).
    • Controlled progression, respecting the pain threshold (the 24 h rule: if pain increases the next day, reduce the intensity).
    • Adapt to the phase: pendulum exercises and gentle mobilisation in phase 1; low-load, long-duration stretching in phase 2; progressive strengthening in phase 3.
  3. Adaptive management of daily activities :
    • Adapt the provocative movements without giving up movement altogether.
    • Support the painful arm at night (a pillow under the elbow).
    • Apply heat before the exercises, ice afterwards if there is post-exertional pain.

When and how should a safe return to sport and to activity be planned?

The return to sport (RTS) or to demanding occupational activity (lifting, overhead work) should be based on objective functional criteria, not on a fixed timescale. The consensus criteria are:5,6

  • Range : passive and active ROM above 90 % of the healthy side, particularly ER and elevation.
  • Strength : isometric cuff strength (Jobe, ER in abduction, lift-off) above 90 % of the other side.
  • Pain : VAS < 2/10 for the movements specific to the sport or the job.
  • Neuromuscular control : no scapular dyskinesis, proprioceptive control of complex movements.
  • Confidence and self-efficacy : assessed by questionnaire (the TSK for fear of movement, for example).

Return-to-sport progression - a criterion-based approach

Adapted from the Kelley 2013 JOSPT CPG and the principles of musculoskeletal RTS

Criterion-based return to sport after frozen shoulder Step 1 Unloaded movement Technical movements without resistance Step 2 Progressive load Bands, light dumbbells Step 3 Intensity and speed Sport simulation Criterion: pain VAS < 2/10 Criterion: strength > 90 % of the healthy side Criterion: motor control OK Step 4 - Competitive return Passive/active ROM > 90 % - Strength > 90 % Confidence and self-efficacy (a low TSK)

Inspired by Kelley MJ et al. JOSPT 2013;43(5):A1-A31 and the principles of musculoskeletal RTS - a criterion-based approach.

The working environment should also be considered. For demanding jobs (manual handling, care work, ceiling work, painting, overhead sports), a graded return with workplace adjustments is often needed for 2-3 months after the thawing phase ends.5

The return to sport follows not a calendar but a functional checklist: range > 90 %, strength > 90 %, pain < 2/10, scapulohumeral control. That approach reduces the risk of recurrence and of secondary injury.

Key points

  • About 40 % of patients still have symptoms in the long term, most often mild (Hand 2008).
  • Guided self-management rests on education about the natural history + a regular HEP + adapting ADLs.
  • Recurrence on the same side is rare (< 5 %), but the other shoulder is affected in 6 to 17 % of patients, above all in people with diabetes (Wong 2017).
  • The return to sport should be based on objective functional criteria (ROM, strength, pain, motor control) and not on a fixed timescale.
  • The stepped approach (unloaded movement -> progressive load -> intensity and speed -> competitive return) is validated.
Bibliography
  1. Vastamaki H, Kettunen J, Vastamaki M. The natural history of idiopathic frozen shoulder. Clin Orthop Relat Res. 2012;470(4):1133-1143. PMID 22090356.
  2. Hand C, Clipsham K, Rees JL, Carr AJ. Long-term outcome of frozen shoulder. J Shoulder Elbow Surg. 2008;17(2):231-236. PMID 17993282.
  3. Lewis J. Frozen shoulder contracture syndrome. Man Ther. 2015;20(1):2-9. PMID 25107826.
  4. Russell S, Jariwala A, Conlon R, et al. A blinded, randomized, controlled trial. J Shoulder Elbow Surg. 2014;23(4):500-507. PMID 24630545.
  5. Kelley MJ, Shaffer MA, Kuhn JE, et al. Shoulder pain and mobility deficits: adhesive capsulitis. J Orthop Sports Phys Ther. 2013;43(5):A1-A31. PMID 23636125.
  6. Wong CK, Levine WN, Deo K, et al. Natural history of frozen shoulder: fact or fiction? Physiotherapy. 2017;103(1):40-47. DOI 10.1016/j.physio.2016.05.009.
  7. Rangan A, Brealey SD, Keding A, et al. UK FROST. Lancet. 2020;396:977-989. PMID 33010843.

What do real clinical cases teach us about frozen shoulder (adhesive capsulitis)?

Three clinical cases published in PubMed Central that illustrate: (1) successful conservative multimodal management (Phansopkar 2023 Cureus, the Spencer technique), (2) a diagnostic trap (Ohta 2017, Parsonage-Turner), (3) a complex case in diabetes treated with hydrodilatation (Dimitri-Pinheiro 2022).

Analysis of a “classic” case: from assessment to resolution.

The case report Phansopkar 2023 (Cureus, PMC10387580) describes a 57-year-old man with a painful, stiff right shoulder for more than six weeks, with lateral rotation of 33° against 80° on the unaffected side. Over three weeks, at five sessions a week, he received moist heat, Codman's pendulum exercises, scapular setting exercises, interferential therapy and the Spencer technique (rotation of the humerus around the elbow used as a pivot, with the arm abducted, then with traction). Pain at rest fell from 7/10 to 0/10 and the SPADI from 72 % to 30 % at six months.1

The diagnostic challenge: when frozen shoulder mimics another condition.

The case published by Ohta 2017 (J Rural Med, PMID 29255532) is that of a 28-year-old woman seen for acute pain in both shoulders, with, from the first examination, wasting of the right deltoid, weakness of every movement of the right shoulder and sensory loss over its lateral aspect. MRI and electromyography confirmed bilateral neuralgic amyotrophy (Parsonage-Turner syndrome). The case is a reminder of the signs that should rule out a diagnosis of frozen shoulder: acute onset, muscle wasting and motor deficit.2

The warning signs that should prompt the diagnosis of frozen shoulder to be reconsidered:2,3

  • Very intense, abrupt initial pain, sometimes preceded by a viral illness.
  • Marked motor weakness, greater than the loss of passive range.
  • Early, visible muscle wasting (deltoid, supraspinatus/infraspinatus, serratus anterior).
  • Failure of well-conducted PT after 6-8 weeks.
  • A territorial distribution of the weakness (suprascapular nerve, long thoracic nerve).

Similarly, calcific tendinopathy can keep a shoulder very painful; a plain shoulder radiograph (AP and lateral) will show it.

A complex case: resistant frozen shoulder in a patient with diabetes.

The retrospective study Dimitri-Pinheiro 2022 (PMC9465918) is an excellent illustration of managing resistant frozen shoulder in the patient with diabetes. A series of patients with diabetes and frozen shoulder refractory to 3-6 months of conventional PT received ultrasound-guided hydrodilatation (injection of 30-40 mL of saline plus corticosteroid plus lidocaine under posterior ultrasound guidance).5

The results show:5

  • An immediate mobility gain (ER, ABD) of the order of 20-30 degrees.
  • Progressive improvement over 6 months with PT continuing.
  • A response that is smaller than in people without diabetes, but clinically significant.
  • A favourable safety profile, provided insulin is adjusted around the procedure.

This kind of case illustrates the treatment escalation strategy : start with PT + HEP + intra-articular corticosteroids in phase 1, then consider hydrodilatation if progress plateaus at 3-6 months, and keep MUA or arthroscopy as a last resort, following UK FROST.6

Red flags from the cases presented

  • Disproportionate motor weakness plus early wasting: rule out Parsonage-Turner (EMG).
  • Very acute pain with calcification on the radiograph: calcific tendinopathy in the resorptive phase.
  • Stalled progress at 3-6 months in the patient with diabetes: consider hydrodilatation before surgical escalation.
  • Any simultaneous bilateral frozen shoulder : a wider aetiological work-up (thyroid, late-onset JIA, other systemic fibroses).
The cases published in PMC remind us of three rules: (1) a solid clinical diagnosis takes priority over imaging, (2) stalled progress means the diagnosis must be reconsidered, (3) in the patient with diabetes, hydrodilatation can create the missing window of opportunity.

Key points

  • The Phansopkar 2023 case (Cureus PMC10387580) describes a favourable course under physiotherapy combining Spencer manual therapy, exercise, heat and electrotherapy; a single case cannot say what worked.
  • The Ohta 2017 case (Parsonage-Turner) is a reminder that acute onset with muscle wasting and motor deficit should rule out a diagnosis of frozen shoulder.
  • The Dimitri-Pinheiro 2022 case series validates ultrasound-guided hydrodilatation in the resistant patient with diabetes.
  • The treatment escalation strategy (PT -> intra-articular corticosteroids -> hydrodilatation -> MUA/arthroscopy) is validated by UK FROST.
Bibliography
  1. Phansopkar P, Qureshi MI. An Integrated Physical Therapy Using Spencer's Technique in the Rehabilitation of a Patient With a Frozen Shoulder: A Case Report. Cureus. 2023;15(6):e41233. PMC10387580.
  2. Ohta R, Shimabukuro A. Parsonage-Turner syndrome in a patient with bilateral shoulder pain: A case report. J Rural Med. 2017;12(2):135-138. PMID 29255532.
  3. Mezian K, Coffey R, Chang KV. Frozen Shoulder. StatPearls. 2023. PMID 29489251.
  4. Wu YC, Tsai WC, Tu YK, Yu TY. Comparative Effectiveness of Nonoperative Treatments for Chronic Calcific Tendinitis of the Shoulder. Arch Phys Med Rehabil. 2017;98(8):1678-1692. PMID 28400182.
  5. Dimitri-Pinheiro S, Pinto BS, Pimenta M, Neves JS, Carvalho D. Influence of diabetes on response to ultrasound guided hydrodistension treatment of adhesive capsulitis: a retrospective study. BMC Endocr Disord. 2022;22(1):227. PMC9465918.
  6. Rangan A, Brealey SD, Keding A, et al. UK FROST. Lancet. 2020;396:977-989. PMID 33010843.
  7. Challoumas D, Biddle M, McLean M, Millar NL. Comparison of Treatments for Frozen Shoulder: A SR and MA. JAMA Netw Open. 2020;3(12):e2029581. DOI 10.1001/jamanetworkopen.2020.29581.
  8. Sun Y, Zhang P, Liu S, et al. Intra-articular Steroid Injection for Frozen Shoulder: A SR and MA of RCTs. Am J Sports Med. 2017;45(9):2171-2179. PMID 28298050.
  9. Chen MH, Chen WS. A Narrative Review of Adhesive Capsulitis with Diabetes. J Clin Med. 2024;13(19):5696. PMID 39407755.

How do you apply these recommendations concretely in your practice?

In this chapter: when and to whom to refer (red flags, reasoning transposed from Finucane 2020; Chester 2018 yellow flags), a reasoned choice of shoulder PROMs (SPADI, DASH, ASES, Constant), the barriers to implementing the evidence (Scurlock-Evans 2014) and audit-and-feedback strategies (Ivers 2012 Cochrane).

When and to which other health professionals should you refer?

Collaborative referral is an essential dimension of practice. The situations calling for medical referral are:

  • The presence of red flags (reasoning transposed from the IFOMPT framework of Finucane 2020, which was built for serious spinal pathology): non-mechanical night pain, weight loss, persistent fever, a history of cancer, progressive neurological involvement, marked inflammatory signs.1
  • Stalled progress at 3-6 months despite well-conducted PT: refer to an orthopaedic surgeon to consider intra-articular corticosteroids, hydrodilatation or surgery.2
  • A suspected alternative diagnosis (Parsonage-Turner, refractory calcific tendinopathy, early inflammatory arthritis): rheumatologist or neurologist.
  • A patient with poorly controlled diabetes (HbA1c > 8 %): diabetologist, for glycaemic optimisation.
  • Significant psychological distress (catastrophising, depression): psychologist or psychotherapist (CBT).3,4

Structured interprofessional collaboration is a determinant of care quality. The key principles include: goals shared with the patient, structured communication between clinicians (a formal physiotherapy report, a letter to the general practitioner), and mutual respect for scopes of practice.5

How do you measure outcomes and overcome barriers to implementation?

Standardised outcome measurement is indispensable for making progress objective and adapting management. For frozen shoulder, the PROMs validated in French and most widely used are:6

PROMItemsScoreMCIDIndication
SPADI13 (5 pain + 8 disability)0-100 (100 = worst)~8-13 pointsThe shoulder reference, sensitive to change
QuickDASH110-100~10 pointsUpper limb, short version
ASES100-100 (100 = best)~6-12 pointsMainly surgical, for postoperative follow-up
Constant-Murley4 domains (pain, ADLs, ROM, strength)0-100 (100 = best)~10 pointsThe surgical standard, requires an examiner
VAS / NRS for pain10-10~2 pointsQuick day-to-day pain tracking

The VAS complements the PROMs: it allows quick day-to-day tracking of pain. Physical performance tests (goniometric ROM measurement, isometric strength testing with a dynamometer) remain indispensable and complete the PROMs for an overall picture.6

Overcoming the barriers to implementing the evidence

The Scurlock-Evans 2014 meta-analysis (Physiotherapy, PMID 24780633) identifies the main barriers to implementing evidence-based practice in physiotherapy:7

  • Lack of time in clinical practice.
  • Difficulty accessing and critically appraising the literature.
  • Lack of organisational support.
  • The gap between the reality of complex patients and the often homogeneous populations of RCTs.

The most effective improvement strategies are:8,9

  • Structured audit and feedback (Ivers 2012 Cochrane): comparing one's practice with evidence-based indicators, followed by constructive feedback.
  • Identifying local leaders (Flodgren 2019 Cochrane) who promote and support the change.
  • Interactive meetings and workshops as continuing education.
  • Decision-support tools built into the practice software.
EBP is not about applying protocols blindly: it is the critical synthesis of the best available evidence, clinical expertise and the patient's values. Frozen shoulder is a good example of where that synthesis makes all the difference.

Key points

  • Refer to a physician where there are red flags (reasoning transposed from Finucane 2020) or where progress stalls at 3-6 months.
  • Collaborate with a diabetologist where control is poor, and with a psychologist where there is catastrophising or depression.
  • Use validated PROMs : the SPADI and QuickDASH are the most practical in the clinic, the ASES and Constant for postoperative follow-up.
  • The barriers to EBP (time, access to the literature) are overcome by audit and feedback (Ivers 2012) and local leaders (Flodgren 2019).
  • EBP is a critical synthesis of evidence, expertise and the patient's values - not the mechanical application of protocols.
Bibliography
  1. Finucane LM, Downie A, Mercer C, et al. International Framework for Red Flags for Potential Serious Spinal Pathologies. J Orthop Sports Phys Ther. 2020;50(7):350-372. DOI 10.2519/jospt.2020.9971.
  2. Rangan A, Brealey SD, Keding A, et al. UK FROST. Lancet. 2020;396:977-989. PMID 33010843.
  3. Chester R, Jerosch-Herold C, Lewis J, Shepstone L. Psychological factors and physiotherapy outcome shoulder pain. Br J Sports Med. 2018;52(4):269-275. PMID 27445360.
  4. Coronado RA, Brintz CE, McKernan LC, et al. Psychologically informed physical therapy. Pain Rep. 2020;5(5):e847. PMID 33490842.
  5. Greenhalgh T, Howick J, Maskrey N. Evidence based medicine: a movement in crisis? BMJ. 2014;348:g3725. PMID 24927763.
  6. Kelley MJ, Shaffer MA, Kuhn JE, et al. Shoulder pain and mobility deficits: adhesive capsulitis. JOSPT. 2013;43(5):A1-A31. PMID 23636125.
  7. Scurlock-Evans L, Upton P, Upton D. Evidence-based practice in physiotherapy: a systematic review of barriers, enablers and interventions. Physiotherapy. 2014;100(3):208-219. PMID 24780633.
  8. Ivers N, Jamtvedt G, Flottorp S, et al. Audit and feedback: effects on professional practice and healthcare outcomes. Cochrane Database Syst Rev. 2012;(6):CD000259. PMID 22696318.
  9. Flodgren G, O Brien MA, Parmelli E, Grimshaw JM. Local opinion leaders: effects on professional practice and healthcare outcomes. Cochrane Database Syst Rev. 2019;(6):CD000125. PMID 31232458.
  10. Geneen LJ, Moore RA, Clarke C, et al. Physical activity and exercise for chronic pain in adults. Cochrane Database Syst Rev. 2017;4(4):CD011279. PMID 28436583.
  11. Hoffmann TC, Légaré F, Simmons MB, et al. Shared decision making: what do clinicians need to know? Med J Aust. 2014;201(1):35-39. DOI 10.5694/mja14.00002.

And after this article?

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Behind this article

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Anthony Baillon, physiotherapist and co-founder of Physio Learning
✍️ Author

Anthony Baillon

Physiotherapist · co-founder of Physio Learning

Marked for life by his first four-hour lecture without a single image, he took a master’s in instructional design so that it would never happen to anyone again. He hunts down publication bias and unreadable slides with the same intransigence.

PhysiotherapistInstructional designerCare design
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Robin Vervaeke, head of scientific content at Physio Learning✓ Verified

Robin Vervaeke

Head of scientific content

Physiotherapist specialising in neuro-musculoskeletal practice and holder of a master’s in public health. He checks the methodological rigour of every article: primary sources, levels of evidence, no exceptions.

Neuro-musculoskeletalMSc Public health
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